Fig 1: CYP-inhibition enhances the nephrotoxicity of OTA. A H&E staining; scale bars 50 µm. B CD45 immunostaining; scale bars 10 µm. C Serum creatinine and blood urea nitrogen. D NGAL and KIM-1 urinary concentrations 24 h after OTA administration with and without ABT compared to vehicle or ABT controls; **p value ≤ 0.01 Tukey’s multiple comparisons test; n = 5 mice per group. The same experimental design as in Fig. 3 was applied
Fig 2: Ttherapeutic efficiency of Cu5.4O USNPs on AKI mice.a Schematic illustration of the establishment and treatment schedule of AKI mice. b Survival curves of AKI mice with different treatment. c Weight variation of AKI mice at 24 h after treatment with Cu5.4O USNPs. Serum levels of d CRE and e BUN in AKI mice at 24 h after different treatment. f H&E staining of kidney tissues from each group. Triangles indicate the formation of casts. g Dihydroethidium (red fluorescence) and DAPI (blue fluorescence) staining of kidney tissues from each group. h SOD, i KIM-1, and j HO-1 levels measured in renal tissue homogenates from each group. In c–e and h–j, data represent means ± s.d. from four independent replicates (***P < 0.001; n.s., no significance, One-way ANOVA). Source data are provided as a Source Data file.
Fig 3: The inhibitory effect of anti-HU1 on the enzymic activities of P4HB. (A) Insulin aggregation assay was performed to determine the activity of recombinant human P4HB. (B) Rb-anti-HU1 (0.15 μg/ml-blue, 0.3 μg/ml-red) inhibited the activity of recombinant human P4HB in a dose dependent manner. (C) The urinary KIM-1 levels in different groups of pristane induced mice ((control, n = 8; KLH, n = 8; KLH-HU1, n = 7). Data are shown as mean ± SD. Statistical analyses were performed with two-tailed unpair Student’s t test using GraphPad Prism 7 software. P >0.05 was considered nonsignificant.
Fig 4: Effect of EGCG (free and encapsulated) pretreatment on (A) serum KIM-1 level, (B) serum NGAL level, (C) NLPR-3 gene expression level, and (D) caspase-1 gene expression level. Data expressed as mean ± SD (n = 8/group), significant difference vs. arespective control, brespective cisplatin group, and crespective free EGCG group each at p ˂ .05.
Fig 5: Increasing PNPT1 expression in mouse renal tubule attenuated tubular injury.a Top, schematic experimental approach of PNPT1-AAV infection in IRI mouse model. Bottom: WB analysis of renal tubular PNPT1 level (3 mice/group). b Left: renal tubular dsRNA (J2, red) staining in IRI mouse model with or without PNPT1 AAV infection. Right: quantification of renal tubular dsRNA level (8 mice/group). c Serum creatinine (top) and urinary KIM-1 levels (bottom) in IRI mouse model with or without PNPT1 AAV infection (5 mice/group). d Top: TUNEL assay of renal tubular apoptosis in IRI model mouse with or without PNPT1 AAV infection. Bottom: quantification of TUNEL assay (5 mice/group). e Top: schematic experimental approach of PNPT1-AAV infection in UUO mouse model. Bottom: WB analysis of renal tubular PNPT1 level (3 mice/group). f Left: renal tubular dsRNA (J2, red) staining in UUO mouse model with or without PNPT1 AAV infection. Right: quantification of renal tubular dsRNA level (8 mice/group). g Serum creatinine (left) and urinary KIM-1 levels (right) in UUO mouse model with or without PNPT1 AAV infection (5 mice/group). h Left: TUNEL assay of renal tubular apoptosis in UUO model mouse with or without PNPT1 AAV infection. Right: quantification of TUNEL assay (5 mice/group). Scale bars, 50 μm. The above experiments were successfully repeated three times. One-way ANOVA with Tukey’s multiple comparisons test was performed in a–h and the results were presented as mean ± SEM. Images of mouse in a, e were created with BioRender.com. Source data are provided as a Source Data file.
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